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. 2017 Sep 2;14:177. doi: 10.1186/s12974-017-0953-z

Fig. 6.

Fig. 6

Chronic phase glibenclamide reduces TNF, BAFF, CCL2, and NOS2 in EAE. a–d Immunolabelings showing white matter of lumbar spinal cord sections from non-EAE control (CTR), untreated EAE mouse (EAE), and EAE mouse treated with glibenclamide starting on pid-24 (EAE + G), examined at pid-40, double immunolabeled for GFAP (red) and either TNF (a), BAFF (b), CCL2 (c) or NOS2 (d) (green); for each molecule, the upper panels show merged images of the color channels at low magnification, and the lower panels show, for the EAE condition, individual color channels and the merged images at high magnification. e Quantification of chromagen immunolabelings for TNF, BAFF, CCL2, and NOS2 in non-EAE controls (CTR), untreated EAE mice (EAE), EAE mice treated with glibenclamide starting on pid-24 (EAE + G), and in global Abcc8−/− mice with induced EAE; original magnification, × 400; 5 mice/group; ## P < 0.01 with respect to non-EAE control (CTR); *P < 0.05 and **P < 0.01 with respect to untreated EAE; scale bars 100 and 25 μm, for upper and lower panels, respectively